We analyzed IL-2 and IL-10 serum levels in 26 HIV-1-infected patients naive of antiretroviral treatment and in 34 patients receiving highly active antiretroviral therapy (HAART). All patients without treatment were asymptomatic. When they were stratified according to levels of CD4+ T cells, IL-2 levels were significantly increased in patients with > or =200 CD4+/microl and IL-10 levels were significantly increased in patients with <200 CD4+/microl compared to controls. A significant negative correlation was observed between IL10 levels and CD4+ T-cell counts. No correlation was observed between IL-2 and IL-10 levels and viral load due to the wide range of variability in the number of HIV copies/ml present in the different patients. However, IL-2 levels were higher in patients with high viral load than in patients with low viral load. In patients with HAART, IL-2 and IL-10 levels were similar to the control group and no differences were detected respecting CD4+ T cells counts and viral load. Our findings show that the modifications in IL-2 and IL-10 serum levels in HIV-1-infected patients naive of antiretroviral treatment are associated with the progression of immunological damage. Furthermore, they show a dysbalance of type-1/type-2 cytokines with an involvement of type-2 cytokines in later stages of HIV infection. Cytokine dysregulation can be reversed by HAART in the context of immune restoration and viral suppression.
BACKGROUND.Oxidative stress in tissues can be provoked by an augmented metabolic rate, which may sometimes be combined with a decrease in the antioxidant capacity. METHODS. In this study we examined the primary enzymatic defense mechanisms against the damage caused by reactive oxygen species (ROS): the superoxide dismutase (SOD) and catalase activities and glutathione content, as well as the levels of total thiobarbituric acidreactant substances (TBARS), indicative of lipid peroxidation. These studies were made in prostate homogenates of rats with experimental autoimmune prostatitis (EAP) and of control rats treated with complete Freund's adjuvant (CFA) or nontreated. RESULTS. The evaluation of antioxidant defenses revealed a significant diminution of the catalase activity in autoimmune rats without changes in SOD activity and glutathione content. TBARS levels evidenced a significant increase in prostate homogenates from autoimmune rats in relation to control rat samples. CONCLUSIONS. The results suggest that in EAP, a marked diminution of catalase activity associated with an enhanced oxidative metabolism of inflammatory macrophages might lead to oxidative damage in this autoimmune disease.
Spontaneous and stimulated reactive oxygen intermediates (ROI) release by peritoneal exudate cells (PEC) and histopathological findings in the prostate gland were assessed during experimental autoimmune prostatitis (EAP) development. Results in EAP rats were compared with data from rats immunized with kidney homogenate, BSA, and CFA, as well as nontreated rats. At 28 days of first immunization (FI), EAP rats spontaneously released significantly more ROI than occurred in the cells from control rats. A similar response was found when ROI release was analyzed after in vitro stimulus. In time course studies, an increased spontaneous O2- production was observed at day 7 after FI, and remained the same during all period studied, (14, 21, and 28 days after FI). The stimulated O2- production showed elevated levels at 7 days after FI and fell afterward to levels similar to those of nontreated rats and increased again at 28 days. Spontaneous or stimulated H2O2 release showed a progressive increase during the study periods. ROI release was correlated with infiltrate formation in the prostate gland. This differential responsiveness could indicate that, during the autoimmune process, the autoantigen(s) amplify the inflammatory response triggered by them.
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